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Biomedical subjects

M Kanzaki

Publications and source records attributed to M Kanzaki.

At least 19 recordsLinked to original sources
PubMed2002

[Total aortic arch replacement for distal aortic arch aneurysm with adhered left lung: report of a case].

A 76-year-old man with a history of pleuritis and a cerebral infarct underwent a total arch replacement for an aneurysm of the distal aortic arch. Computed tomography revealed a true aneurysm having a maximum diameter of 70 mm as well as pleural thickening and calcification. Total arch replacement with selective cerebral perfusion was performed through median sternotomy and left thoracotomy. The myocardial ischemic time was shortened by reperfusion from the right axillary artery after the anastomosis of the proximal ascending aorta and the brachiocephalic artery. After the other branches of the arch were anastomosed, a distal anastomosis through the left thoracotomy was then performed using the pull-through method, enabling minimal decortication of the adhered lung. Our surgical procedure for distal arch aneurysm with adhered lung involves the addition of a left thoracotomy, but the reduction in the myocardial ischemic time and lung injury are of benefit.

Aged↗
PubMed2002

[Corrective surgery for pectus excavatum in patients with Marfan syndrome].

OBJECTIVE: Among 1,967 patients who underwent corrective surgery for pectus excavatum in our department between January 1980 and December 2001, 33 patients diagnosed as having Marfan syndrome were evaluated. We evaluated the clinical problems and outcome of the 33 patients. RESULTS: The outcome of corrective surgery for pectus excavatum in the 26 patients who underwent a single technique surgery was generally good. Pectus excavatum was complicated by a total of 25 cases of cardiovascular disorder in 14 of 33 (42%) patients. Six patients underwent corrective surgery for pectus excavatum and cardiovascular disorders simultaneously. Three patients also had disorders of lung, which included spontaneous pneumothorax in 2 patients and progressive emphysematous cyst in 1 patient. The 2 patients with spontaneous pneumothorax underwent resection of bullae together with corrective surgery of pectus excavatum, while the patient with progressive emphysematous cyst underwent resection of bullae in a separate surgery after correction of pectus excavatum. Cardiovascular disorders were aggravated in 6 of the 20 patients who could be follow up. A total of 4 (20%) patients died long after surgery. CONCLUSIONS: We corrected pectus excavatum in 33 patients with Marfan syndrome, and obtained favorable outcomes. The postsurgical outcome depends on progression of lesions of the heart and large vessels, and it is essential to monitor such lesions carefully.

Adolescent↗
PubMed2002

[Surgical management of acute empyema].

Basic principles apply to the management of all forms of acute empyema: investigation and treatment of the underlying infection, drainage of purulent collection, obliteration of the space, and treatment of the associated intercurrent medical conditions. From July 1999 to May 2001, we performed surgical treatment in 11 patients for acute empyema. There were 4 cases of the fibrinopurulent phase and 7 cases of the organizing phase. Surgical procedure was 7 open thoracotomies and 4 thoracoscopies. The mean operating time was 154.2 +/- 36.6 minutes and blood loss during surgery was 344.7 +/- 274.8 ml. There was no procedure-related morbidity. In conclusion, early aggressive surgical approach is a feasible method for treatment of acute empyema.

Acute Disease↗
PubMed2001

Insulin stimulates actin comet tails on intracellular GLUT4-containing compartments in differentiated 3T3L1 adipocytes.

Incubation of isolated GLUT4-containing vesicles with Xenopus oocyte extracts resulted in a guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) and sodium orthovanadate stimulation of actin comet tails. The in vitro actin-based GLUT4 vesicle motility was inhibited by both latrunculin B and a dominant-interfering N-WASP mutant, N-WASP/Delta VCA. Preparations of gently sheared (broken) 3T3L1 adipocytes also displayed GTP gamma S and sodium orthovanadate stimulation of actin comet tails on GLUT4 intracellular compartments. Furthermore, insulin pretreatment of intact adipocytes prior to gently shearing also resulted in a marked increase in actin polymerization and actin comet tailing on GLUT4 vesicles. In addition, the insulin stimulation of actin comet tails was completely inhibited by Clostridum difficile toxin B, demonstrating a specific role for a Rho family member small GTP-binding protein. Expression of N-WASP/Delta VCA in intact cells had little effect on adipocyte cortical actin but partially inhibited insulin-stimulated GLUT4 translocation. Taken together, these data demonstrate that insulin can induce GLUT4 vesicle actin comet tails that are necessary for the efficient translocation of GLUT4 from intracellular storage sites to the plasma membrane.

Actins↗
PubMed2001

Insulin-stimulated GLUT4 translocation in adipocytes is dependent upon cortical actin remodeling.

Rhodamine-labeled phalloidin staining of morphologically differentiated 3T3L1 adipocytes demonstrated that F-actin predominantly exists juxtaposed to and lining the inner face of the plasma membrane (cortical actin) with a smaller amount of stress fiber and/or ruffling actin confined to the cell bottom in contact with the substratum. The extent of cortical actin disruption with various doses of either latrunculin B or Clostridium difficile toxin B (a Rho family small GTP-binding protein toxin) directly correlated with the inhibition of insulin-stimulated glucose uptake and GLUT4 translocation. The dissolution of the cortical actin network had no significant effect on proximal insulin receptor signaling events including insulin receptor autophosphorylation, tyrosine phosphorylation of insulin receptor substrate and Cbl, or serine/threonine phosphorylation of Akt. Surprisingly, however, stabilization of F-actin with jasplakinolide also resulted in a dose-dependent inhibition of insulin-stimulated glucose uptake and GLUT4 translocation. In vivo time-lapse confocal fluorescent microscopy of actin-yellow fluorescent protein demonstrated that insulin stimulation initially results in cortical actin remodeling followed by an increase in polymerized actin in the peri-nuclear region. Importantly, the insulin stimulation of cortical actin rearrangements was completely blocked by treatment of the cells with latrunculin B, C. difficile toxin B, and jasplakinolide. Furthermore, expression of the dominant-interfering TC10/T31N mutant completely disrupted cortical actin and prevents any insulin-stimulated actin remodeling. Together, these data demonstrate that cortical actin, but not stress fibers, lamellipodia, or filopodia, plays an important regulatory role in insulin-stimulated GLUT4 translocation. In addition, cortical F-actin does not function in a static manner (e.g. barrier or scaffold), but insulin-stimulated dynamic cortical actin remodeling is necessary for the GLUT4 translocation process.

3T3 Cells↗
PubMed2001

Lipid raft microdomain compartmentalization of TC10 is required for insulin signaling and GLUT4 translocation.

Recent studies indicate that insulin stimulation of glucose transporter (GLUT)4 translocation requires at least two distinct insulin receptor-mediated signals: one leading to the activation of phosphatidylinositol 3 (PI-3) kinase and the other to the activation of the small GTP binding protein TC10. We now demonstrate that TC10 is processed through the secretory membrane trafficking system and localizes to caveolin-enriched lipid raft microdomains. Although insulin activated the wild-type TC10 protein and a TC10/H-Ras chimera that were targeted to lipid raft microdomains, it was unable to activate a TC10/K-Ras chimera that was directed to the nonlipid raft domains. Similarly, only the lipid raft-localized TC10/ H-Ras chimera inhibited GLUT4 translocation, whereas the TC10/K-Ras chimera showed no significant inhibitory activity. Furthermore, disruption of lipid raft microdomains by expression of a dominant-interfering caveolin 3 mutant (Cav3/DGV) inhibited the insulin stimulation of GLUT4 translocation and TC10 lipid raft localization and activation without affecting PI-3 kinase signaling. These data demonstrate that the insulin stimulation of GLUT4 translocation in adipocytes requires the spatial separation and distinct compartmentalization of the PI-3 kinase and TC10 signaling pathways.

Adipocytes↗
PubMed2001

Insulin-stimulated GLUT4 translocation requires the CAP-dependent activation of TC10.

The stimulation of glucose uptake by insulin in muscle and adipose tissue requires translocation of the GLUT4 glucose transporter protein from intracellular storage sites to the cell surface. Although the cellular dynamics of GLUT4 vesicle trafficking are well described, the signalling pathways that link the insulin receptor to GLUT4 translocation remain poorly understood. Activation of phosphatidylinositol-3-OH kinase (PI(3)K) is required for this trafficking event, but it is not sufficient to produce GLUT4 translocation. We previously described a pathway involving the insulin-stimulated tyrosine phosphorylation of Cbl, which is recruited to the insulin receptor by the adapter protein CAP. On phosphorylation, Cbl is translocated to lipid rafts. Blocking this step completely inhibits the stimulation of GLUT4 translocation by insulin. Here we show that phosphorylated Cbl recruits the CrkII-C3G complex to lipid rafts, where C3G specifically activates the small GTP-binding protein TC10. This process is independent of PI(3)K, but requires the translocation of Cbl, Crk and C3G to the lipid raft. The activation of TC10 is essential for insulin-stimulated glucose uptake and GLUT4 translocation. The TC10 pathway functions in parallel with PI(3)K to stimulate fully GLUT4 translocation in response to insulin.

Adipocytes↗
PubMed2001

The role of video-assisted thoracoscopic surgery in the diagnosis of the small peripheral pulmonary nodule.

BACKGROUND: The use of imaging techniques to detect small peripheral pulmonary nodules often results in a missed diagnosis. Thoracoscopy had limited application until recently, when advances in technology allowed thoracic surgeons greater visualization and mobility within the chest. METHODS: Between September 1992 and June 1997, 81 patients were treated for small peripheral pulmonary nodules by pulmonary wedge excision using video-assisted thoracoscopic techniques. The patients were 39 men and 42 women with an average age of 59.5 years. RESULTS: A definitive diagnosis was obtained in all cases. Malignancies were found in 44 patients (55%), which involved primary lung cancer in 28 patients and metastatic lesions in 16 patients. The rate of malignancy in nodules measuring 1 cm or less was 18%. There was no operative mortality or morbidity. CONCLUSIONS: We conclude that video-assisted thoracoscopic lung biopsy is a more effective and less invasive diagnostic tool for small peripheral pulmonary nodules.

Female↗
PubMed2001

Identification of a novel chloride channel expressed in the endoplasmic reticulum, golgi apparatus, and nucleus.

MID-1 is a Saccharomyces cerevisiae gene encoding a stretch-activated channel. Using MID-1 as a molecular probe, we isolated rat cDNA encoding a protein with four putative transmembrane domains. This gene encoded a protein of 541 amino acids. We also cloned the human homologue, which encoded 551 amino acids. Messenger RNA for this gene was expressed abundantly in the testis and moderately in the spleen, liver, kidney, heart, brain, and lung. In the testis, immunoreactivity of the gene product was detected both in the cytoplasm and the nucleus. When expressed in Chinese hamster ovary cells, the gene product was located in intracellular compartments including endoplasmic reticulum and the Golgi apparatus. When microsome fraction obtained from the transfected cells, but not from mock-transfected cells, was incorporated into the lipid bilayer, an anion channel activity was detected. Unitary conductance was 70 picosiemens in symmetric 150 mm KCl solution. We designated this gene Mid-1-related chloride channel (MCLC). MCLC encodes a new class of chloride channel expressed in intracellular compartments.

Amino Acid Sequence↗
PubMed2001

Nitinol stent for the treatment of tracheobronchial stenosis.

OBJECTIVE: The purpose of this study was to evaluate the potential utility of implantation of a nickel-titanium alloy (nitinol) stent for the treatment of malignant or benign tracheobronchial stenosis. METHODS: We evaluated 18 patients (14 men and 4 women) who received 24 nitinol stents, between November 1997 and May 2000. All 18 patients had severe dyspnea caused by tracheobronchial stenosis. The underlying condition was malignant disease in 15 patients, and benign tracheal collapse in the other 3 patients. RESULTS: Implantation of the stent was successfully performed in all patients. Seventeen patients experienced immediate clinical improvement in respiratory symptoms. The remaining 1 patient with a bronchial fistule after lobectomy did not benefit, and died of pneumonia at 16 days after the implantation. In 15 patients, the procedure was performed using a flexible bronchoscope under local anesthesia alone, while the remaining 3 patients needed intravenous sedation. There was no complication resulting from the stent implantation. Among the 3 patients with benign tracheal collapse, 2 patients were alive at 746 and at 401 days after the stent implantation, at the time of this report. One patient with cicatricial stenosis after intubation died of heart failure due to previous myocardial infarction. Among the 15 patients with malignant disease, 4 patients have survived for 177 to 305 days to date, while the other 11 patients have died of primary malignancy with a mean survival duration of 60.2 days. CONCLUSION: The nitinol stent was effective in treating malignant or benign tracheobronchial stenosis, and had some remarkable advantages compared with other tracheobronchial stents. In stenting, most procedures can be performed using flexible bronchoscope under local anesthesia.

Adult↗
PubMed2001

Y-chromosome microdeletion and phenotype in cytogenetically normal men with idiopathic azoospermia.

OBJECTIVE: To determine the prevalence of microdeletions of the long arm of chromosome Y within the AZFa, AZFb, and AZFc subregions in patients with idiopathic azoospermia, and then correlate the microdeletions with clinical phenotypes to determine the most important subregion for screening. DESIGN: Controlled clinical study. SETTING: Male infertility clinic, Kobe University Hospital. PATIENT(S): Among 89 consecutive azoospermic patients, those whose infertility was related to known hereditary, endocrine, or obstructive causes or a cytogenetic abnormality were excluded; 54 remaining patients were studied using a polymerase chain reaction (PCR). Of these patients, 33 had Sertoli cell only syndrome, 10 had maturation arrest, and 11 had hypospermatogenesis. INTERVENTION(S): Blood and semen samples and testicular biopsies were obtained from all of the participants. MAIN OUTCOME MEASURE(S): We performed semen analysis, polymerase chain amplification of 28 DNA loci on the long arm of the Y chromosome involving the DAZ (deleted in azoospermia), and measured the plasma FSH, LH, testosterone, prolactin, and estradiol levels. RESULT(S): Microdeletions were detected in 14 of the 54 patients (nine with Sertoli cell only, three with maturation arrest, and two with hypospermatogenesis). Most microdeletions involved AZFb or AZFc. Patients with hypospermatogenesis or maturation arrest showed deletion only in AZFc. The DAZ gene was deleted in four patients with Sertoli cell only and one patient with maturation arrest. The RBM gene was deleted in two patients with Sertoli cell only who had particularly large deletions, but in no patients with arrest or hypospermatogenesis. CONCLUSION(S): Cytogenetically azoospermic patients should be examined for microdeletions before undertaking assisted reproduction. AZFc may be the most important subregion to screen. In addition, intact AZFa and AZFb subregions may be important for the presence of germ cells.

Adult↗
PubMed2001

Significance of serum inhibin B concentration for evaluating improvement in spermatogenesis after varicocelectomy.

BACKGROUND: The study aim was to clarify the relationship of serum inhibin B concentrations to recovery of spermatogenic function after varicocelectomy, both as a predictor of improvement in the seminogram and as a means of monitoring hormonal function after surgery. METHODS: Fifty-two varicocele patients, including five with normal sperm concentrations, were studied. Changes in the seminogram, serum hormone concentrations and serum inhibin B were evaluated in the 47 oligozoospermic patients after surgery. Preoperative inhibin B concentrations correlated significantly with serum concentrations of FSH (r = 0.598, P < 0.0001) and testosterone (r = 0.380, P < 0.02). Inhibin B concentrations also correlated significantly with sperm concentration (r = 0.351, P < 0.02) and total testicular volume (r = 0.578, P < 0.0001). No significant correlation was seen between inhibin B and the Johnsen score. Preoperative concentrations of inhibin B were higher in patients who increased their sperm concentration after surgery (responders) than in those without improved concentrations (non-responders). No significant difference was observed between pre- and postoperative inhibin B concentrations in responders or non-responders. However, 15 of 25 (60%) patients with increased inhibin B showed improvement of the seminogram, while only five of 22 (23%) patients with no change or a decrease in inhibin B had any improvement (P < 0.05). CONCLUSIONS: Preoperative serum inhibin B concentration could not reliably predict a response to varicocelectomy. However, a change in serum inhibin B concentration after varicocelectomy might be helpful to evaluate the improvement of testicular function after varicocelectomy.

Adult↗
PubMed2001

Signal integration and the specificity of insulin action.

Insulin is a potent metabolic hormone essential for the maintenance of normal circulating blood glucose level in mammals. The physiologic control of glucose homeostasis results from a balance between hepatic glucose release (glycogenolysis and gluconeogenesis) and dietary glucose absorption versus skeletal muscle and adipose tissue glucose uptake and disposal. Disruption of this delicate balance either through defects in insulin secretion, liver glucose output, or peripheral tissue glucose uptake results in pathophysiological states of insulin resistance and diabetes. In particular, glucose transport into skeletal muscle and adipose tissue is the rate-limiting step in glucose metabolism and reduction in the efficiency of this process (insulin resistance) is one of the earliest predictors for the development of Type II diabetes. Importantly, recent studies have directly implicated an impairment in insulin receptor signal transduction as the prime mechanism for peripheral tissue insulin resistance. In this review, we have focused on recent developments in our understanding of the molecular mechanisms and signal transduction pathways that insulin utilizes to specifically regulate glucose uptake. The detailed understanding of these events will provide a conceptual framework for the development of new therapeutic targets to treat this chronic and debilitating disease process.

Adipose Tissue↗
PubMed2001

Effects of suspension of air-conditioning on airtight-type racks.

Although isolation racks are superior to open-type racks in terms of securing breeding conditions for laboratory animals, the contingency-proofing capability of the former has yet to be determined. Therefore, from the view of risk management, we studied the environmental change in isolation racks by forcibly suspending ventilation and air-conditioning and confirming the maximal time length for complete recovery to the original condition after restarting their operations. The isolation racks were placed in a room that was equipped with an independent air-conditioning system. When the inside condition of the racks reached 22-24 degrees C and 59-64% of relative humidity, the air-conditioning and ventilation were forcibly suspended and the subsequent temperature, relative humidity, ammonium and CO2 concentrations in the racks were measured over time. We found that after suspending the air-conditioning and ventilation, it took 40-60 min for temperature, and about 10 min for relative humidity to exceed the maximum values (temperature and relative humidity) referred to in the Showa 58 Nenban Guideline Jikken Doubutsu Shisetsu no Kenchiku oyobi Setsubi (Guidelines of buildings and facilities for experimental animals in Japan; Year 1983 edition). After 17 hr 25 min of the suspension of air-conditioning and ventilation, two rats were found dead. Then, the air-conditioning and ventilation were restarted. It took about 2 hr for temperature, and 50 min for relative humidity to regain the guideline values. The ammonium concentration stayed within the guideline value with a maximum concentration of 2 ppm in the experimental period, whereas the CO2 concentration was found to exceed 9% at the time of animal death.

Air Conditioning↗
PubMed2000

CAP defines a second signalling pathway required for insulin-stimulated glucose transport.

Insulin stimulates the transport of glucose into fat and muscle cells. Although the precise molecular mechanisms involved in this process remain uncertain, insulin initiates its actions by binding to its tyrosine kinase receptor, leading to the phosphorylation of intracellular substrates. One such substrate is the Cbl proto-oncogene product. Cbl is recruited to the insulin receptor by interaction with the adapter protein CAP, through one of three adjacent SH3 domains in the carboxy terminus of CAP. Upon phosphorylation of Cbl, the CAP-Cbl complex dissociates from the insulin receptor and moves to a caveolin-enriched, triton-insoluble membrane fraction. Here, to identify a molecular mechanism underlying this subcellular redistribution, we screened a yeast two-hybrid library using the amino-terminal region of CAP and identified the caveolar protein flotillin. Flotillin forms a ternary complex with CAP and Cbl, directing the localization of the CAP-Cbl complex to a lipid raft subdomain of the plasma membrane. Expression of the N-terminal domain of CAP in 3T3-L1 adipocytes blocks the stimulation of glucose transport by insulin, without affecting signalling events that depend on phosphatidylinositol-3-OH kinase. Thus, localization of the Cbl-CAP complex to lipid rafts generates a pathway that is crucial in the regulation of glucose uptake.

3T3 Cells↗
PubMed2000

The trimeric GTP-binding protein (G(q)/G(11)) alpha subunit is required for insulin-stimulated GLUT4 translocation in 3T3L1 adipocytes.

To investigate the potential role of trimeric GTP-binding proteins regulating GLUT4 translocation in adipocytes, wild type and constitutively active G(q) (G(q)/Q209L), G(i) (G(i)/Q205L), and G(s) (G(s)/Q227L) alpha subunit mutants were expressed in 3T3L1 adipocytes. Although expression of neither the wild type nor G(i)/Q205L and G(s)/Q227L alpha subunit mutants had any effect on the basal or insulin-stimulated translocation of a co-expressed GLUT4-enhanced green fluorescent protein (EGFP) fusion protein, expression of G(q)/Q209L resulted in GLUT4-EGFP translocation in the absence of insulin. In contrast, microinjection of an inhibitory G(q)/G(11) alpha subunit-specific antibody but not a G(i) or G(s) alpha subunit antibody prevented insulin-stimulated endogenous GLUT4 translocation. Consistent with a required role for GTP-bound G(q)/G(11), expression of the regulators of G protein signaling (RGS4 and RGS16) also attenuated insulin-stimulated GLUT4-EGFP translocation. To assess the relationship between G(q)/G(11) function with the phosphatidylinositol 3-kinase dependent pathway, expression of a dominant-interfering p85 regulatory subunit, as well as wortmannin treatment inhibited insulin-stimulated but not G(q)/Q209L-stimulated GLUT4-EGFP translocation. Furthermore, G(q)/Q209L did not induce the in vivo accumulation of phosphatidylinositol-3,4,5-trisphosphate (PIP(3)), whereas expression of the RGS proteins did not prevent the insulin-stimulated accumulation of PIP(3). Together, these data demonstrate that insulin stimulation of GLUT4 translocation requires at least two independent signal transduction pathways, one mediated through the phosphatidylinositol 3-kinase and another through the trimeric GTP-binding proteins G(q) and/or G(11).

3T3 Cells↗
PubMed2000

Nitric oxide production of rat Leydig and Sertoli cells is stimulated by round spermatid factor(s).

In this study, we provide evidence of cell-to-cell interaction between rat germ cells and Leydig or Sertoli cells in relation to nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) expression. As a result of being cultured in a round spermatid-conditioned medium (RSd-CM), NO production in both Leydig and Sertoli cells increased in proportion to the length of the culture period. iNOS mRNA expression in both types of cells also increased in a dose-dependent manner as a result of being cultured with RSd-CM. This increase was detected as early as 3 h and was maintained up to 24 h. In contrast, neither NO production nor iNOS mRNA increased in either type of cell following culture in a pachytene spermatocyte-conditioned medium (PS-CM). Our findings suggest that RSd may control NO production of Leydig and Sertoli cells. This cell-to-cell interaction may be an important mechanism of regulation of testicular function.

Animals↗